ライフサイエンスコーパス: DNFB

1 DNFB sensitization of CD154(-/-) mice primed IFN-gamma-p

2 DNFB treatment also resulted in rapid depletion of appro

3 DNFB-driven chronic ACD was marked by type 2 inflammatio

4 DNFB-sensitized IL-1R(-/-) mice had low CHS responses to

5 th an equimolar mixture of DNFB and [(2)H(3)]DNFB.

6 In accordance, DNFB-induced ear swelling was reduced by approximately 5

7 After DNFB treatment, Gr-1(high) neutrophils and F4/80(+) macr

8 inflammatory cytokines and chemokines after DNFB treatment revealed robust changes in genes that are

9 lated IL-10 mRNA as early as 3-6 hours after DNFB application, immediately preceding a decrease of IL

10 Although DNFB sensitization of gld/perforin-/- mice induced hapte

11 wing exposure to DNFB in wild-type mice, and DNFB-induced ear swelling is reduced by approximately 50

12 In contrast, applying DNFB to PAF receptor-deficient mice or mice injected wit

13 njection of stromelysin-1 immediately before DNFB sensitization rescued the impaired CHS response to

14 Application of both DNFB and DNTB induced apoptotic cell death of DC in the

15 Oral tolerance was induced by DNFB gavage in germ-free and mice deficient in several T

16 Oral tolerance induced by DNFB gavage was impaired in germ-free mice and TLR4-defi

17 inhibition of subsequent CHS to the chemical DNFB in wild-type, but not in PAF-R-deficient mice.

18 application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to the development

19 ponse, induced by 2,4,-dinitrofluorobenzene (DNFB), in P-selectin-deficient mice.

20 BALB/c mice, both 2,4-dinitrofluorobenzene (DNFB) and FITC induce CHS.

21 amino groups with 2, 4-dinitrofluorobenzene (DNFB) coupled with electrospray ionization mass spectrom

22 l for CHS in which 2,4-dinitrofluorobenzene (DNFB) is used as allergen, we found that gammadelta T ce

23 f BALB/c mice with 2,4-dinitrofluorobenzene (DNFB) or oxazolone (Ox) resulted in increased and prolon

24 atinase B (MMP-9) in a dinitrofluorobenzene (DNFB)-induced model of contact hypersensitivity (CHS).

25 t its related compound dinitrofluorobenzene (DNFB), because DNTB-pretreated mice cannot be sensitized

26 ensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site,

27 e strains of mice when dinitrofluorobenzene (DNFB) is applied to an irradiated skin surface.

28 vity (CHS) responses to dintrofluorobenzene (DNFB) are IFN-gamma-producing CD8(+) T cells, whereas CD

29 Transient TGFbeta1 induction during DNFB sensitization increased contact hypersensitivity re

30 from mice treated with anti-CD154 mAb during DNFB sensitization were less stimulatory for hapten-prim

31 BTLA(-/-) mice showed enhanced DNFB-induced CHS and proliferation and IFN-gamma product

32 FITC/DNFB skin painting and subsequent enzyme-linked immunosp

33 naling during 2, 4 dinitro-1-fluorobenezene (DNFB) sensitization to induce hapten-specific CD8 effect

34 in response to 2,4-dinitro-1-fluorobenzene (DNFB) required Fas ligand (FasL) and perforin expression

35 tact sensitizer 2,4-dinitro-1-fluorobenzene (DNFB) resulted in a 13-fold increase in CCL27 protein ac

36 tact sensitizer 2,4 dinitro-1-fluorobenzene (DNFB) to normal skin.

37 Applying 2,4-dinitro-1-fluorobenzene (DNFB) to wild-type mice activated LC migration.

38 (CK) inhibitor 2,4-dinitro-1-fluorobenzene (DNFB).

39 ontact sensitizer 2,4-dinitro-fluorobenzene (DNFB) depends on microbiota/TLRs and evaluated the role

40 nse in a model of 2,4-dinitro-fluorobenzene (DNFB)-induced contact hypersensitivity.

41 By contrast, following DNFB application to UV-irradiated skin (UV+DNFB), IL-12p

42 4/80+CD11c(-) cells in DLN 3 hours following DNFB application.

43 e ability of intestinal dendritic cells from DNFB-fed mice to inhibit ACD on adoptive transfer.

44 nnot be sensitized against the potent hapten DNFB.

45 Topical application of a reactive hapten, DNFB, augmented dSEARCH and triggered lateral migration

46 rease in MBL2 cell apoptosis was detected in DNFB-treated ears compared with vehicle control.

47 tin contributes to generation of immunity in DNFB-induced contact hypersensitivity.

48 cytokine-secreting cells remained reduced in DNFB-sensitized mice, even when the animals were rechall

49 n inflammation by one topical application of DNFB following MBL2 inoculation in C57BL/6 mice resulted

50 osomes blocked the tumor-promoting effect of DNFB.

51 rance was detected by applying 185 microg of DNFB epicutaneously to mice treated 2 wk earlier with a

52 are derivatized with an equimolar mixture of DNFB and [(2)H(3)]DNFB.

53 Lymphocytes from lymph nodes of DNFB-sensitized stromelysin-1-deficient mice did not pro

54 plications of ARN077 attenuated key signs of DNFB-induced dermatitis in a dose-dependent manner.

55 uated the impact of topically applied THC on DNFB-mediated allergic contact dermatitis in wild-type a

56 estinal migratory CD103(+) DCs carrying oral DNFB, especially the CD103(+)CD11b(+) DC subset expressi

57 as well as immunologic tolerance to a second DNFB immunization through normal skin.

58 In vivo injection of 6A6 suppressed DNFB-induced CHS and IFN-gamma production of CD8(+) T ce

59 subchronic applications of ARN077 suppressed DNFB-induced inflammation when administered either befor

60 We show that DNFB triggers DETC activation and IL-1beta production in

61 The DNFB-regulated tumor formation was blocked by early, but

62 when administered either before or after the DNFB challenge.

63 However, the DNFB response is Th1-predominant, while the FITC respons

64 IL-17, these T cells did not infiltrate the DNFB challenge site to elicit CHS but did infiltrate the

65 e trafficking of the effector T cells to the DNFB challenge site to elicit the response were investig

66 TCs appear in the skin following exposure to DNFB in wild-type mice, and DNFB-induced ear swelling is

67 had no defect in their ability to respond to DNFB.

68 h IL-12 before DNTB application responded to DNFB challenge with a pronounced ear swelling response w

69 ization rescued the impaired CHS response to DNFB in stromelysin-1-deficient mice.

70 icient mice showed a reduced CHS response to DNFB, in bone marrow chimera and adoptive transfer exper

71 MyD88 were unable to mount a CHS response to DNFB.

72 D88 signaling pathway in the CHS response to DNFB.

73 Similar CHS responses to DNFB were elicited in wild-type and CD154(-/-) animals.

74 g response without previous sensitization to DNFB, showing that IL-12 can convert the tolerogen DNTB

75 ermate wild-type (WT) mice were subjected to DNFB-induced CHS, severe combined immunodeficient (SCID)

76 R4 conditions induction of oral tolerance to DNFB through licensing tolerogenic gut DCs.

77 ion induced long-lasting unresponsiveness to DNFB, with 88% and 76% inhibition of primary (first chal

78 a markedly impaired CHS response to topical DNFB, although they responded normally to cutaneously ap

79 Eliciting an immune reaction towards DNFB in wild-type mice, followed by adoptive transfer to

80 alone did not upregulate IL-10 mRNA, but UV+DNFB upregulated IL-10 mRNA as early as 3-6 hours after

81 g DNFB application to UV-irradiated skin (UV+DNFB), IL-12p40 mRNA was not upregulated, and DLN IL-12p

82 or scratching behavior after challenge with DNFB, confirming that this enzyme plays an important rol

83 even when the animals were rechallenged with DNFB.

84 Sensitization with DNFB or Ox induced lymph node cell populations of CD8+ T

85 ocytes produce IL-1beta when stimulated with DNFB.

86 e recipient mice adoptively transferred with DNFB immunity generated in P-selectin-deficient mice.

87 ificantly lower than in animals treated with DNFB or IL-12 plus DNTB.

88 ated animals compared with mice treated with DNFB or IL-12 plus DNTB.

89 tory T cells isolated from mice treated with DNFB, DNTB, or IL-12 followed by DNTB.

90 After treatment with DNFB, PCr withdrawal had no effect on the Ca2+ transient